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Supplement: International Research Conference on Food, Nutrition, and Cancer

The Dietary Phytochemical Chlorophyllin Alters E-Cadherin and ß-Catenin Expression in Human Colon Cancer Cells¹–^,3

Linus Pauling Institute, Oregon State University, Corvallis, OR 97331

⁴To whom correspondence should be addressed. E-mail: Rod.Dashwood{at}oregonstate.edu.

Chlorophyllin (CHL), an anticarcinogenic and antimutagenic water-soluble derivative of chlorophyll, has been reported to induce apoptosis in human colon cancer cells via a pathway involving cell differentiation. Induction of differentiation markers may be important in limiting cancer-cell invasion and metastasis, and there is much interest in understanding the underlying mechanisms, because this might provide insights for cancer chemotherapy. In the present study, human HCT116 colon-cancer cells were treated with CHL, and the expression levels of E-cadherin and ß-catenin were examined using immunocytochemistry and laser scanning confocal microscopy. E-cadherin was detected almost exclusively at the cell periphery of cancer cells treated with or without CHL, but the expression of E-cadherin in the plasma membrane was markedly elevated in the cells treated with CHL. ß-Catenin also was strongly expressed in the plasma membrane, especially after CHL treatment. No change in the expression of ß-catenin mRNA was detected across a broad range of CHL concentrations (10–500 µmol/L), but there was a concentration-dependent decrease in nuclear ß-catenin protein levels without overt changes in the cytosolic pool of ß-catenin. Our interpretation of these findings is that CHL induces E-cadherin expression, and this facilitates trafficking of ß-catenin away from the nucleus and into the plasma membrane, possibly for destruction via the adherins junction remodeling (Hakai) pathway.

KEY WORDS: • colon cancer • chemoprevention • adherins junctions

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